The ultimate stem cell, the oocyte, is frequently very large. For example, Drosophila and Xenopus oocytes are approximately 10(5) times larger than normal somatic cells. Importantly, once the large oocytes are fertilized, the resulting embryonic cells proliferate rapidly. Moreover, these divisions occur in the absence of cell growth and are not governed by normal cell cycle controls. Observations suggest that mitogens and cell growth signals modulate proliferation by upregulating G1-phase cyclins, which in turn promote cell division. Like embryonic cells, the proliferation of cancer cells is largely independent of mitogens and growth factors. This occurs, in part, because many proteins that are known to modulate G1-phase cyclin activity are frequently mutated in cancer cells. Interestingly, we have found that both the expression and the activity of G1-phase cyclins is modulated by growth rate and cell size in yeast. These and other data suggest that proliferative capacity correlates with cell size. Thus, a major goal of our laboratory is to use yeast to investigate the relationship between proliferation rate, G1-phase cyclins, growth rate, and cell size. The elucidation of this relationship will help clarify the role of cell size in promoting proliferation in both normal and cancer cells.
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Evidence ID | Analyze ID | Gene/Complex | Systematic Name/Complex Accession | Qualifier | Gene Ontology Term ID | Gene Ontology Term | Aspect | Annotation Extension | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Phenotype | Experiment Type | Experiment Type Category | Mutant Information | Strain Background | Chemical | Details | Reference |
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Evidence ID | Analyze ID | Gene | Gene Systematic Name | Disease Ontology Term | Disease Ontology Term ID | Qualifier | Evidence | Method | Source | Assigned On | Reference |
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Evidence ID | Analyze ID | Regulator | Regulator Systematic Name | Target | Target Systematic Name | Direction | Regulation of | Happens During | Regulator Type | Direction | Regulation Of | Happens During | Method | Evidence | Strain Background | Reference |
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Site | Modification | Modifier | Source | Reference |
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Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Allele | Assay | Annotation | Action | Phenotype | SGA score | P-value | Source | Reference | Note |
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Increase the total number of rows showing on this page by using the pull-down located below the table, or use the page scroll at the table's top right to browse through the table's pages; use the arrows to the right of a column header to sort by that column; filter the table using the "Filter" box at the top of the table; click on the small "i" buttons located within a cell for an annotation to view further details about experiment type and any other genes involved in the interaction.
Evidence ID | Analyze ID | Interactor | Interactor Systematic Name | Interactor | Interactor Systematic Name | Assay | Annotation | Action | Modification | Source | Reference | Note |
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Complement ID | Locus ID | Gene | Species | Gene ID | Strain background | Direction | Details | Source | Reference |
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Evidence ID | Analyze ID | Dataset | Description | Keywords | Number of Conditions | Reference |
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